Treatment Of Cirrhosis Of The Liver By A Nutritious Diet And Supplements Rich In Vitamin B Complex

[Wilfrid]

Thanks, I posted about this one before: Quinogerm B complex (vitamines B naturelles) - 60 gélules végétales

It's a very good product, I used to buy it in the past.
Another french lab called Vecteur Santé use B vitamins extract from buckwheat germ in all of their products containing B vitamins.

 

[Wagner83]

It's a very good product, I used to buy it in the past.
Another french lab called Vecteur Santé use B vitamins extract from buckwheat germ in all of their products containing B vitamins.

Did you notice something from supplementing it?

 

[Wilfrid]

Did you notice something from supplementing it?

As well as I can remember not really. I took four capsules in divided dosages and didn't notice any positive nor negative results.

 

[Amazoniac]

@Amazoniac , @haidut

What do you think about this product:
Liver Extract - BIOFAC A/S

Wilfrid! I can only think of this.

 

[Wilfrid]

Wilfrid! I can only think of this.

Damn!

 

[haidut]

@Amazoniac , @haidut

What do you think about this product:
Liver Extract - BIOFAC A/S

It should be a good product if it is of bovine origin. My impression is that porcine liver is not very healthy as food and contains a lot of PUFA due to how the pigs are fed. I don't know if anybody has asked Peat abut porcine liver, so it would be interesting to hear his opinion as well.

 

[Amazoniac]

Regime for Treatment of Severe and Acute Liver Disease

"The diseased liver cell required cystine to prevent necrosis but could not utilize it adequately from external sources. The problem, therefore, was to render the cells less sensitive to cystine deficiency, so that they could utilize their own cystine until such time as recovery was complete enough to allow them to use the amino-acids of surrounding tissue fluid. From this point of view the role assigned to tocopherol in the production of experimental hepatic necrosis (Schwarz, 1944; Gyorgy [not the one above], 1947; Himsworth and Lindan, 1949) assumes great importance. This vitamin has therefore been included in the regime of treatment described below.

The intracellular oxidative processes of the liver and other organs also require other vitamins. In their absence toxic products accumulate which could easily be a factor in the final death of liver cells. The successful application of massive doses of the vitamin-B group in the cholaemia of cirrhosis has already been reported (Patek et al., 1948). This form of therapy was therefore also included in the regime."

 

[Amazoniac]

Not about inulin, so, useless:
- T3 as a primary hepatic @Mito gen - Anton Bungay
- Thyroid Hormone Metabolism During Liver Regeneration in Rats
- The influence of hypothyroidism on liver regeneration: an experimental study in rats

 

[Amazoniac]

The effects of dietary methionine restriction on morphology and function of the liver and brain (!)

"Methionine restriction has a profound effect on lipid and glucose metabolism in the liver resulting in increased insulin sensitivity and reduced risk of diabetes mellitus, hypertension and NAFLD [25,54]. In human population limited methionine intake may also be used for achievement of metabolic fitness. Interestingly, methionine restriction causes hyperphagia in rodents, but with weight loss, decreased adiposity and increased energy expenditure [55]. Similar findings were also evident in humans and after 16 weeks of restricted intake of methionine, body weight and adiposity were found to be decreased, while insulin sensitivity of the tissues was increased [56]. In the liver methionine restricted diet alleviates steatosis [25,57] and delays the development of inflammation in an NF-κB dependent manner."

"[..]methionine restriction does not induce mitochondrial biogenesis, but increases the aerobic capacity of mitochondria [61]."

"[..]methionine restriction has a direct and autonomous effect on insulin signaling in the liver. The proposed mechanism of insulin-sensitizing effect of methionine restricted diet in the liver is through GSH depletion, which limits the capacity of hepatocytes to reactivate oxidized phosphatase and tensin homologue (PTEN). This ultimately leads to increased concentration of phosphatidylinositol-(3,4,5)-triphosphate (PIP3), which then activates Akt [57]."

"Interestingly, in contrast to pure methionine restriction, combined methionine and choline restriction have prooxidant, proinflammatory effects in the liver [92,93] and may even promote the development of liver cirrhosis [94] and hepatocellular carcinoma [95]. Methionine- and choline-deficient (MCD) diet in mice also induces liver steatosis and may be used as a suitable model for investigation of the pathophysiological mechanisms of NAFLD [96]. In 2 weeks MCD diet induces focal microvesicular liver steatosis, while in 6 weeks inflammation accompanies diffuse micro- to macrovesicular steatosis with increased serum level of C-reactive protein [93]. These changes are associated with increased levels of malondialdehyde and nitrites+nitrates and reduced GSH level, thus indicating that MCD diet causes oxidative and nitrosative stress in the liver. Additionally, the antioxidative capacity of the liver was found to be decreased by MCD diet due to the reduction of superoxide dismutase and catalase activities, the reduction being the most extensive after 4 week-treatment with MCD diet [93]. Lack of methionine and choline in the diet was also found to cause alterations in free fatty acid profile in the liver [92]. Within 2 weeks it causes a decline in palmitic, stearic, arachidonic and docosahexaenoic acid (DHA). The significance of this finding should be further investigated, but a decrease in DHA level may at least partially contribute to the proinflammatory effect of MCD diet on the liver [92]. All of these changes are dominantly caused by choline deficiency. However, although choline deficiency is sufficient for the development of steatosis, both methionine and choline deficiency are essential for the development of inflammation in the liver [97]. These findings clearly indicate, that adequate intake of micronutrients according to daily requirements is a prerequisite for beneficial effects of dietary methionine restriction on metabolic processes and function of the liver."

 

[Antonello]

There is another option here in Europe made from quinoa seeds
Vitamin B 180er
Hovewer those natural b complex all contains B12 that is not naturally present in plants so even if they said no additives no synthetic ecc...they put it that cobalamin in it somehow

 

[BigChad]

@Amazoniac @Travis

If one made a mistake and supplemented 20-40mg ferrous bisglycinate capsules for a few weeks, as well as took 250mg green tea extract capsules 3x a week for a year straight, do you have advice on how to heal the liver damage caused by those supplements? Would high protein intake and vitamin MK4/MK7 a few times a week be enough to heal the liver? What else could be done as far as supplements or diet, to help the liver heal

 

[Amazoniac]

@Amazoniac @Travis

If one made a mistake and supplemented 20-40mg ferrous bisglycinate capsules for a few weeks, as well as took 250mg green tea extract capsules 3x a week for a year straight, do you have advice on how to heal the liver damage caused by those supplements? Would high protein intake and vitamin MK4/MK7 a few times a week be enough to heal the liver? What else could be done as far as supplements or diet, to help the liver heal

The iron is not a concern in this regard:
- Possible Iron Overload


Was is the extract consumed is with meals? Are lab tests abnormal? Eggs are a good idea if you enjoy them.

- Safety of Green Tea Extracts

"Green tea has been consumed for centuries by different cultures around the world. In addition to its use as a beverage, green tea consumption has increased because of putative health benefits. Recently, several concentrated extracts of green tea have appeared on the market as weight loss and sports supplements. These extracts are formulated to contain higher concentrations of EGCG or caffeine. To put this into perspective, a cup of green tea can provide 80–106 mg of polyphenols. Although 1–3 cups per day may be a common consumption level in the US, ingestion of as many as 9 cups per day of tea is not uncommon in Japan, according to epidemiological studies.[58] Green tea extracts are often standardized to polyphenol levels that vary from 25% to 97%. For example, the suggested dose of an extract standardized to 25% catechins (Exolise®, one capsule three times daily) provides 375 mg catechins per day, of which 270 mg is EGCG. This is roughly the equivalent of three cups of tea. Another product (Tegreen 97®) is standardized to 97% polyphenols with a recommended serving that provides nearly 600 mg polyphenols per day."​

- Hepatotoxicity from green tea: a review of the literature and two unpublished cases

"The bioavailability of catechins after oral administration is low: EGCG levels detected in plasma correspond to 0.2–2.0% of the ingested amount [47]; however, catechin plasma levels can increase under particular conditions. Isbrucker et al. found that the plasma area under the curve (AUC) for EGCG was significantly higher in fasted (205.7 ng h/mL) than in pre-fed dogs (19.8 ng h/mL) after 2 weeks dosing at 300 mg/kg per day by dietary administration [48]. The same authors did not observe adverse effects when 500 mg/kg per day EGCG were administered for 13 weeks to pre-fed dogs; conversely, this dose caused morbidity when administered to fasted dogs [48]. Other studies in healthy volunteers showed that after the administration of 800 mg Polyphenon E, a decaffeinated extract of green tea containing 60% EGCG, the plasma Cmax of free EGCG in the fasting condition was more then fivefold higher than that obtained after administration of the same dose with food [49]. Finally, Ullman et al. showed that after repeated administrations of EGCG 800 mg/day, the Cmax was 1682 ng/mL on day 1 and 2431 ng/mL on day 10 [50]."

"(-)-Epigallocatechin gallate cytotoxicity and ROS formation increased significantly by dicumarol, a NAD(P)H:quinone oxidoreductase 1 (NQO1) inhibitor, thus suggesting that o-quinone metabolites of EGCG cause cytotoxicity and are reductively detoxified by NQO1 [53]. Treatment with the catechol-O-methyltranferase inhibitor, entacapone, was also found to cause a significant increase in EGCG cytotoxicity and ROS formation, thus suggesting that hepatocyte methylation plays a role in detoxifying this compound [53]. According to Sang et al., catehol-O-methyltranferase can protect cells from EGCG-mediated oxidative stress and hepatotoxicity by methylation at the 4’- and 4”-hydroxyl groups, both of which are possible sites for quinone formation and redox cycling [55]."​

 

[BigChad]

The iron is not a concern in this regard:
- Possible Iron Overload


Was is the extract consumed is with meals? Are lab tests abnormal? Eggs are a good idea if you enjoy them.

- Safety of Green Tea Extracts

"Green tea has been consumed for centuries by different cultures around the world. In addition to its use as a beverage, green tea consumption has increased because of putative health benefits. Recently, several concentrated extracts of green tea have appeared on the market as weight loss and sports supplements. These extracts are formulated to contain higher concentrations of EGCG or caffeine. To put this into perspective, a cup of green tea can provide 80–106 mg of polyphenols. Although 1–3 cups per day may be a common consumption level in the US, ingestion of as many as 9 cups per day of tea is not uncommon in Japan, according to epidemiological studies.[58] Green tea extracts are often standardized to polyphenol levels that vary from 25% to 97%. For example, the suggested dose of an extract standardized to 25% catechins (Exolise®, one capsule three times daily) provides 375 mg catechins per day, of which 270 mg is EGCG. This is roughly the equivalent of three cups of tea. Another product (Tegreen 97®) is standardized to 97% polyphenols with a recommended serving that provides nearly 600 mg polyphenols per day."​

- Hepatotoxicity from green tea: a review of the literature and two unpublished cases

"The bioavailability of catechins after oral administration is low: EGCG levels detected in plasma correspond to 0.2–2.0% of the ingested amount [47]; however, catechin plasma levels can increase under particular conditions. Isbrucker et al. found that the plasma area under the curve (AUC) for EGCG was significantly higher in fasted (205.7 ng h/mL) than in pre-fed dogs (19.8 ng h/mL) after 2 weeks dosing at 300 mg/kg per day by dietary administration [48]. The same authors did not observe adverse effects when 500 mg/kg per day EGCG were administered for 13 weeks to pre-fed dogs; conversely, this dose caused morbidity when administered to fasted dogs [48]. Other studies in healthy volunteers showed that after the administration of 800 mg Polyphenon E, a decaffeinated extract of green tea containing 60% EGCG, the plasma Cmax of free EGCG in the fasting condition was more then fivefold higher than that obtained after administration of the same dose with food [49]. Finally, Ullman et al. showed that after repeated administrations of EGCG 800 mg/day, the Cmax was 1682 ng/mL on day 1 and 2431 ng/mL on day 10 [50]."

"(-)-Epigallocatechin gallate cytotoxicity and ROS formation increased significantly by dicumarol, a NAD(P)H:quinone oxidoreductase 1 (NQO1) inhibitor, thus suggesting that o-quinone metabolites of EGCG cause cytotoxicity and are reductively detoxified by NQO1 [53]. Treatment with the catechol-O-methyltranferase inhibitor, entacapone, was also found to cause a significant increase in EGCG cytotoxicity and ROS formation, thus suggesting that hepatocyte methylation plays a role in detoxifying this compound [53]. According to Sang et al., catehol-O-methyltranferase can protect cells from EGCG-mediated oxidative stress and hepatotoxicity by methylation at the 4’- and 4”-hydroxyl groups, both of which are possible sites for quinone formation and redox cycling [55]."​

yeah the extract was consumed with meals. usually after a cup of green tea actually. it was 250mg green tea extract, I believe 95% polyphenols and 95% catechins.
blood tests showed "normal kidney and liver function" but I don't really trust the blood tests, I wanted to get a liver and kidney ultrasound to be sure.
the reactions I get from olive leaf extract and taurine are similar. It seems that they cause a die off of toxins and the toxins are too great for my liver to clear them. that is something that seemed to imply slow/compromised liver function. i have no allergies to taurine or olive leaf, no excepients in the products (just veggie capsule) and the olive leaf extract actually uses standardized extract not crushed olive leaf powder so there is no risk of birch pollen or allergens in it. the reaction only seems to appear after consuming 500mg olive leaf extract 25% oleupurein or 1000mg taurine. it seems that my liver function is weak due to the supplements usage before or simply hypothyroidism itself slowing down the liver function. the effects I got from OLE and taurine seem to be unheard of.

 

[NathanK]

This is interesting, Mr. Amazon

It is my understanding that chronic diseased tissue/illness generates or worsens malnutrition, in a vicious cycle manner since the person ends up not being able to eat or digest food enough and utilize nutrients optimally, whilst the injured tissue imposes ever increasing nutritional needs the worse it gets.

So, in 1941 albumin below 4.0 was considered low. Nowaways the bottom value of the range is 3.5 or so, yikes! Maybe this "adjustment" reflects that more and more people in society are getting liver dysfunction. Peat was right on that one.

This was me for years (except that my pulse was predominantly low, not rapid... more exactly, erratic). How can a person know if they have cirrhosis if it is not always clinically evident? Also, I've read having liver enzymes in the "normal" range doesn't exclude the possibility of liver disease.

An ALT disproportionately higher to AST can be indicative of fatty liver. A follow up with ultrasound will confirm. No need for an MRI or biopsy

 

[Bart1]

The effects of dietary methionine restriction on morphology and function of the liver and brain (!)

"Methionine restriction has a profound effect on lipid and glucose metabolism in the liver resulting in increased insulin sensitivity and reduced risk of diabetes mellitus, hypertension and NAFLD [25,54]. In human population limited methionine intake may also be used for achievement of metabolic fitness. Interestingly, methionine restriction causes hyperphagia in rodents, but with weight loss, decreased adiposity and increased energy expenditure [55]. Similar findings were also evident in humans and after 16 weeks of restricted intake of methionine, body weight and adiposity were found to be decreased, while insulin sensitivity of the tissues was increased [56]. In the liver methionine restricted diet alleviates steatosis [25,57] and delays the development of inflammation in an NF-κB dependent manner."

"[..]methionine restriction does not induce mitochondrial biogenesis, but increases the aerobic capacity of mitochondria [61]."

"[..]methionine restriction has a direct and autonomous effect on insulin signaling in the liver. The proposed mechanism of insulin-sensitizing effect of methionine restricted diet in the liver is through GSH depletion, which limits the capacity of hepatocytes to reactivate oxidized phosphatase and tensin homologue (PTEN). This ultimately leads to increased concentration of phosphatidylinositol-(3,4,5)-triphosphate (PIP3), which then activates Akt [57]."

"Interestingly, in contrast to pure methionine restriction, combined methionine and choline restriction have prooxidant, proinflammatory effects in the liver [92,93] and may even promote the development of liver cirrhosis [94] and hepatocellular carcinoma [95]. Methionine- and choline-deficient (MCD) diet in mice also induces liver steatosis and may be used as a suitable model for investigation of the pathophysiological mechanisms of NAFLD [96]. In 2 weeks MCD diet induces focal microvesicular liver steatosis, while in 6 weeks inflammation accompanies diffuse micro- to macrovesicular steatosis with increased serum level of C-reactive protein [93]. These changes are associated with increased levels of malondialdehyde and nitrites+nitrates and reduced GSH level, thus indicating that MCD diet causes oxidative and nitrosative stress in the liver. Additionally, the antioxidative capacity of the liver was found to be decreased by MCD diet due to the reduction of superoxide dismutase and catalase activities, the reduction being the most extensive after 4 week-treatment with MCD diet [93]. Lack of methionine and choline in the diet was also found to cause alterations in free fatty acid profile in the liver [92]. Within 2 weeks it causes a decline in palmitic, stearic, arachidonic and docosahexaenoic acid (DHA). The significance of this finding should be further investigated, but a decrease in DHA level may at least partially contribute to the proinflammatory effect of MCD diet on the liver [92]. All of these changes are dominantly caused by choline deficiency. However, although choline deficiency is sufficient for the development of steatosis, both methionine and choline deficiency are essential for the development of inflammation in the liver [97]. These findings clearly indicate, that adequate intake of micronutrients according to daily requirements is a prerequisite for beneficial effects of dietary methionine restriction on metabolic processes and function of the liver."

Thank you for creating this thread. It is very informative for me since I think I am in a beginning stage if cirrhosis. I have hemochromatosis which probably caused it.

In this post you bring up an important point. In Peat land we talk about restricting methionine. How do you suggest to balance methionine, since it can both be damaging in excess and a deficiency? Or don’t you agree with dr Peat that methionine is bad in excess?

 

[Amazoniac]

Thank you for creating this thread. It is very informative for me since I think I am in a beginning stage if cirrhosis. I have hemochromatosis which probably caused it.

In this post you bring up an important point. In Peat land we talk about restricting methionine. How do you suggest to balance methionine, since it can both be damaging in excess and a deficiency? Or don’t you agree with dr Peat that methionine is bad in excess?

I would lean towards restriction because not only it's harmful in excess, but its metabolism tends to become impeded in liver issues. Not sure if homocysteine is always a reliable marker, but if you have it elevated, at least you know that some methionine is being converted.

Adenosylated methionine (immediate metabolite in methylation cycle) can be tried for diagnostic purposes. If you feel great with it, it justifies intensifying the restriction and supporting the downstream metabolites that are possibly deficient for depending on something that's not working right. In this case, it's worth taking easy on choline and cobalamin/folate because they might worsen the accumulation of methionine (circulating level can be tested too, but it's not as common as homocysteine). Supplementing creatine, magnesium (methionine to adenosylmethionine consumes ATP), pyridoxine, taurine and sulfate are probably good ideas. Do you consume enough manganese (I know it's not important, but it's for fun) and molybdenum?

Extreme protein restriction is going to tax the liver further. Casein is great, but the cysteine content is relatively low, therefore you'll be counting on the conversion above to be functioning decently. Given that some people don't tolerate it well, experimenting with civilized amounts of a good whey is something to consider. Gelatin as well.
- Amino Acid Content And Profile Of Some Proteinaceous Foods (I regret having rushed and not verifying these values at the time because now I don't know if they're correct)

There's a difference between decreasing protein consumption because the person wants or has to, the latter is not a noble reason. When it can't be used properly, it's reasonable to lower it to minimize the stress, yet what was disturbing prior to restriction might be there afterwards; it can put the person at risk of serious deficiency, in particular because at the low end people are probably avoiding the concentrated sources of protein that are easier to digest, making them overestimate how much they're obtaining.

You may find something useful in Gerson's approach (fixing the liver was a priority) and here (for alternatives that decrease requirements).

 

[Bart1]

I would lean towards restriction because not only it's harmful in excess, but its metabolism tends to become impeded in liver issues. Not sure if homocysteine is always a reliable marker, but if you have it elevated, at least you know that some methionine is being converted.

Adenosylated methionine (immediate metabolite in methylation cycle) can be tried for diagnostic purposes. If you feel great with it, it justifies intensifying the restriction and supporting the downstream metabolites that are possibly deficient for depending on something that's not working right. In this case, it's worth taking easy on choline and cobalamin/folate because they might worsen the accumulation of methionine (circulating level can be tested too, but it's not as common as homocysteine). Supplementing creatine, magnesium (methionine to adenosylmethionine consumes ATP), pyridoxine, taurine and sulfate are probably good ideas. Do you consume enough manganese (I know it's not important, but it's for fun) and molybdenum?

Extreme protein restriction is going to tax the liver further. Casein is great, but the cysteine content is relatively low, therefore you'll be counting on the conversion above to be functioning decently. Given that some people don't tolerate it well, experimenting with civilized amounts of a good whey is something to consider. Gelatin as well.
- Amino Acid Content And Profile Of Some Proteinaceous Foods (I regret having rushed and not verifying these values at the time because now I don't know if they're correct)

There's a difference between decreasing protein consumption because the person wants or has to, the latter is not a noble reason. When it can't be used properly, it's reasonable to lower it to minimize the stress, yet what was disturbing prior to restriction might be there afterwards; it can put the person at risk of serious deficiency, in particular because at the low end people are probably avoiding the concentrated sources of protein that are easier to digest, making them overestimate how much they're obtaining.

You may find something useful in Gerson's approach (fixing the liver was a priority) and here (for alternatives that decrease requirements).

Thanks, I will investigate further on your suggestions!

 

[gaze]

this was a great thread. i'm gonna follow the semi liquid diet tomo for fun, but instead of brewers yeast i'm gonna use nutritional yeast and im gonna boil water and put a tablespoon in so the sediment falls to the bottom. also i'm not gonna eat that many eggs